Healthcare workers experience moral injury (MI), a violation of their moral code due to circumstances beyond their control. MI threatens the healthcare workforce in all settings and leads to medical errors, depression/anxiety, and personal and occupational dysfunction, significantly affecting job satisfaction and retention. This article aims to differentiate concepts and define causes surrounding MI in healthcare. A narrative literature review was performed using SCOPUS, CINAHL, and PubMed for peer-reviewed journal articles published in English between 2017 and 2023. Search terms included “moral injury” and “moral distress,” identifying 249 records. While individual risk factors predispose healthcare workers to MI, root causes stem from healthcare systems. Accumulation of moral stressors and potentially morally injurious events (PMIEs) (from administrative burden, institutional betrayal, lack of autonomy, corporatization of healthcare, and inadequate resources) result in MI. Individuals with MI develop moral resilience or residue, leading to burnout, job abandonment, and post-traumatic stress. Healthcare institutions should focus on administrative and climate interventions to prevent and address MI. Management should ensure autonomy, provide tangible support, reduce administrative burden, advocate for diversity of clinical healthcare roles in positions of interdisciplinary leadership, and communicate effectively. Strategies also exist for individuals to increase moral resilience, reducing the impact of moral stressors and PMIEs.

Background: Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death worldwide and is poorly predicted with current risk estimation tools. The biological mechanisms relating ASCVD risk factors to oxidative stress (OS) and how this accumulates ASCVD risk are misunderstood. Purpose: To develop a comprehensive conceptual model explaining how expanded clinical, social, and genetic ASCVD risk factors accumulate ASCVD risk through OS. Conclusions: OS (primarily from excess reactive oxygen species) and inflammation are present along the entire ASCVD pathophysiologic continuum. An expanded list of clinical and social ASCVD risk factors (including hypertension, obesity, diabetes, kidney disease, inflammatory diseases, substance use, poor nutrition, psychosocial stress, air pollution, race, and genetic ancestry) influence ASCVD largely through increased OS. Many risk factors exert a positive feedback mechanism to increase OS. One genetic risk factor, haptoglobin (Hp) genotype, is associated with higher ASCVD risk in diabetes and hypothesized to do the same in those with insulin resistance due to the Hp 2-2 genotype increasing OS. Implications: Understanding the biological mechanisms of OS informs how these ASCVD risk factors relate to each other and compound ASCVD risk. Individualized ASCVD risk estimation should include a comprehensive, holistic perspective of risk factors to better address the clinical, social, and genetic influences of OS. Preventing and reducing OS is key to preventing ASCVD development or progression.

The complex interplay of increased atherogenic lipoproteins, inflammation, and immune activation hallmarks the pathogenesis of atherosclerotic cardiovascular disease (ASCVD). Atherosclerotic cardiovascular disease remains a leading cause of death, yet risk estimator tools lack comprehensiveness for genetic/inflammatory biomarkers associated with ASCVD. Unexplained ASCVD risk necessitates a better understanding of primary, secondary, and tertiary prevention variables. This article discusses the clinical utility of genetic and inflammatory biomarkers for ASCVD risk prediction, management, treatment, and recategorization into primary, secondary, and tertiary prevention. Furthermore, nurse practitioners (NPs) should use a ternary prevention classification system instead of the current binary system to mitigate risk in the large group of patients with subclinical ASCVD. High-sensitivity C-reactive protein (hs-CRP)—linearly associated with ASCVD—and lipoprotein-associated phospholipase-A2 (Lp-PLA2) and myeloperoxidase (MPO), both associated with plaque vulnerability/rupture, are inflammatory biomarkers. Elevated hs-CRP, MPO, and Lp-PLA2 treatment requires addressing root causes of elevation (e.g., obesity, insulin resistance, tobacco use, gingival disease, and chronic autoimmune/infectious conditions). In addition, haptoglobin (Hp) phenotype determines the antioxidant potential of Hp. Haptoglobin phenotype, a root cause of ASCVD, is a one-time test. Individuals with Hp 2-2 should adopt a gluten-free diet to reduce endothelial and intestinal inflammation. Nurse practitioners should use stricter glycemic goals (hemoglobin A1c ≤6.5%) and add daily vitamin E if this group has type 2 diabetes. Genetic/inflammatory biomarkers should be used to better predict ASCVD risk and tailor primary, secondary, and tertiary prevention treatment. Clinical use of these biomarkers reaches beyond the standard of care to reduce residual ASCVD risk.

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